Abstract: The main differences are reflected in the discoveries that: (i) the
non-nucleoside reverse transcriptase inhibitor resistance mutation,
V106M, has been seen in subtype C and CRF01_AE, but not in subtype B, (ii) the
protease inhibitor mutations
L89I/V have been reported in C, F and G subtypes, but not in B, (iii) a nelfinavir selected non-
D30N containing pathway predominated in CRF01_AE and CRF02_AG, while the emergence of
D30N is favoured in subtypes B and D, (iv) studies on thymidine analog-treated subtype C infections from South Africa, Botswana and Malawi have reported a higher frequency of the
K65R resistance mutation than that typically seen with subtype B.Additionally, some substitutions that seem to impact non-B viruses differentially a